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AA Y4 Finals cards NE > Dermatology > Flashcards

Dermatology Flashcards

1
Q

what is the similarity and difference between macule and patches?

A

both are hyper pigmented flat lesions

a macule is <1cm

a patch is >1cm

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2
Q

what is the difference between a macule and a papule

A

macule is flat

papule is raised

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3
Q

what is the difference between a nodule and a papule

A

both are raised, well defined lesions

papules are <0.5cm

nodules are >0.5cm

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4
Q

what is the difference between a vesicle and a bulla

A

both are fluid filled lesions

vesicles are <0.5cm

Bulla are >0.5cm

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5
Q

what skin layer does a wound have to go down to to be classed as an ulcer

A

dermis

ulcer is a skin break that descends to the level of the dermis

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6
Q

what is the underlying cause of conditions that show purpura

A

low platelets (eg. von willebrand disease)

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7
Q

put the following topical steroids in order from least to most potent:

betnovate, hydrocortisone, dermovate, eumovate

A
  1. hydrocortisone
  2. eumovate
  3. betnovate
  4. dermovate
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8
Q

which condition can topical steroids cause a flare up of?

A

Psoriasis

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9
Q

what are the 3 functions of keratinocytes

A

produce keratin
absorb vit D
immune functions

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10
Q

name the 4 layers of the epidermis, from deepest to superficial?

A

basal layer
prickle cell layer
granular layer
keratin layer

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11
Q

on average, how long does it take a keratinocyte to travel from the basal cell layer to the keratin layer?

A

28 days

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12
Q

what are the non-nucleated remnants of keratinocytes found in the keratin layer called?

A

corneocytes

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13
Q

where do melanocytes migrate from? what is their role

A

the neural crest

produce melanin from tyrosine

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14
Q

what layer are langerhan cells found?

what is their primary function and their main distinguishing feature?

A

the prickle cell layer

main function: antigen presentation to T cells

distinguishing feature: Birkbeck granules

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15
Q

in terms of layers of the skin, what causes formation of bullae (pemphigoid)

A

diseases that cause alterations of the demo-epidermal junction

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16
Q

what is the primary function of the dermis?

A

to cushion and support the epidermis

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17
Q

what specific feature of the blood supply to the dermis allows for adequate thermoregulation?

A

the blood supply far outweighs metabolic demand

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18
Q

what is the difference in role between meissners corpuscles and pancinian corpuscles?

A

meissners corpuscles: found high in dermis, respond to light touch and vibration

pancinian corpuscles: found deeper in the dermis and respond to deep, heavy pressure

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19
Q

which cells are responsible for vit D production

A

keratinocytes

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20
Q

bullous pemphigoid is an autoimmune condition. Describe what the antibodies attack and what this results in

A

BP is a T2 hypersensitivity reaction

antibodies are produced against the hemi-desmosome proteins

hemi-desmosome proteins act as an anchor between the epidermis and basement membrane

BP results in interruption of the demo-epidermal junction and sub-epidermal blisters

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21
Q

what is the main differentiating factor between bullous pemphigoid and pemphigus?

A

whether there is mucosal involvement or not…

pemphigoid= no mucosal involvement (means the mouth is spared)

pemphigus= mucosal involvement

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22
Q

where do the blisters in bullous pemphigoid typically arise? how do they present

A

usually affect flexures of proximal limbs or trunk

large, tense, itchy blisters

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23
Q

what is nikolsky’s sign? is it positive or negative in bullous pemphigoid?

A

positive sign= when the top layers of the skin slip away from the lower layers when rubbed

nikolsky’s sign is negative in BP

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24
Q

how is bullous pemphigoid diagnosed?

what can be seen on immunofluorescence?

A

biopsy: sub epidermal blisters and inflammatory markers
immunofluorescence: linear IgG and complement (C3) along basement membrane

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25
Q

how is bullous pemphigoid managed?

A

local disease: high potency topical steroids

systemic: oral steroids +/- tetracyclines +/- anti-histamine

last resort: immunosupression

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26
Q

pemphigus vulgaris is an autoimmune condition. what protein are the antibodies produced against?

what is the function of this protein?

A

desmoglien 3

it is one of the desmosome proteins involved in cell-cell adhesions

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27
Q

compare the blisters seen in bullous pemphigoid and pemphigus vulgaris?

A

the blisters in pemphigus vulgaris are intra-epidermal

they are therefore much weaker and burst easier than bullous phemphigoid

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28
Q

describe the blisters seen in pemphigus vulgaris?

is the mucous membrane affected

A

multiple, painful, flaccid, fragile blisters

mucous membrane is affected- there are blisters in the mouth, conjunctiva, vulva

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29
Q

is nikolsky’s sign positive or negative in pemphigus vulgaris?

A

nikolsky’s sign +ive (blisters are intra-epidermal)

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30
Q

what can be seen on biopsy in pemphigus vulgaris?

A

acantholysis- separation of individual keratinocytes

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31
Q

which blistering condition causes “chicken wire deposition of IgG within the epidermis”

A

pemphigus vulgaris

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32
Q

how is pemphigus vulgaris treated?

A

local disease: topical steroids

systemic disease: oral steroids +/- immunosupression +/- rituximab

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33
Q

dermatitis herpetiformis is an AI skin condition. what antibody is produced?

what other disease process involves this antibody?

A

anti-TTG

coeliac disease

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34
Q

compare the site of blisters in pemphigoid vulgaris, bullous phemphigoid and dermatitis herpetiformis?

A

sub-epidermal: bullous pemphigoid and dermatitis herpetiformis

intra-epidermal: pemphigoid vulgaris

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35
Q

compare the locations of blisters in bullous pemphigoid and dermatitis herpetiformis (ie- flexor or extensor)

A

flexors: BP
extensors: dermatitis herpetiformis

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36
Q

describe characteristics of the itch in dermatitis herpetiformis

A

intensely itchy blisters

the itch can precede the blisters

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37
Q

how is dermatitis herpetiformis investigated? what do results show?

A

bloods: anti-TTG
biopsy: sub epidermal blisters with papillary microabscesses

immunofluorescence

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38
Q

what can be seen on immunofluorescence in dermatitis herpetiformis?

A

granular deposits of IgA within the papillae of epidermis

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39
Q

which blistering condition shows IgG and which shows IgA on immunofluorescence?

A

IgG = bullous pemphigoid

IgA= dermatitis herpetiformis

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40
Q

how is dermatitis herpetiformis managed?

A

1st line: gluten free diet +/- dapsone

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41
Q

what is a rare complication of dermatitis herpetiformis

A

increased risk of small bowel lymphoma

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42
Q

how many peaks in incidence is there in psoriasis?

A

2 peaks

1 in 20 y/o’s

1 in 50y/o’s

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43
Q

which drugs can cause psoriasis?

A

B Blockers, lithium, anti-malarial drugs, swift withdrawal of topical or systemic steroids

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44
Q

in psoriasis, what does the increased epidermal proliferation result in?

A

hyperkeratosis: thickening of the keratin cell layer
parakeratosis: retention of nuclei in corneocytes

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45
Q

why does psoriasis cause parakeratosis (retention of the nuclei in corneocytes)

A

the increased proliferation reduces the time cells are allowed for migration and differentiation

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46
Q

what happens to the layers of the epidermis in psoriasis

A

absence of the granular layer

thickening of the prickle cell layer

munro abscesses: neutrophil filled abscesses within the statum corneum

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47
Q

name the 2 main pathological processes in psoriasis?

A
  1. increased epidermal proliferation

2. dilation and proliferation of dermal blood vessels (causes accumulation of immune cells, esp T cells)

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48
Q

what clinical sign is seen in psoriasis due to the dilated blood vessels? what is this clinical sign?

A

Auspitz sign

when the plaque is scraped away, there is pinpoint bleeding due to dilated blood vessels

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49
Q

what is the most common type of psoriasis

A

chronic plaque

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50
Q

does plaque psoriasis affect extensors or flexors?

A

usually extensors

eczema is more likely to affect flexors

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51
Q

what is koebner phenomenon, seen in psoriasis?

A

when psoriatic plaques develop at site of trauma 2-6 weeks after trauma has occurred

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52
Q

when is guttate psoriasis seen? what age group does it tend to affect?

A

tends to follow an infection, especially strep throat

affects younger patients, 15-25 y/o’s

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53
Q

which type of psoriasis is pear-dropped in shape?

A

guttate psoriasis

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54
Q

how is guttate psoriasis managed?

A

self limiting- resolves in 6 weeks

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55
Q

which type of psoriasis can be precipitated by removal of potent steroids?

A

erythrodermic psoriasis

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56
Q

which type of psoriasis can result in complete failure of the skin?

A

erythrodermic psoriasis- the plaques fall off in large sheets

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57
Q

what is considered 1st line topical therapy in psoriasis to reduce the rate of cell devision?

A

vitamin D analogues - calcitriol

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58
Q

in which forms of psoriasis are steroids used?

A

palmo-plantar and flexural disease

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59
Q

which areas of the body does flexural psoriasis tend to affect?

A

develops in the groin, axilla or under the breasts

mostly in the elderly

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60
Q

what do NICE recommend as 1st line treatment in psoriasis?

A

potent corticosteroid alongside a vitamin D analogue for up to 4 weeks

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61
Q

what do NICE say is the 2nd line treatment for psoriasis management?

A

increase dose of vit D analogue

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62
Q

what is considered the longest duration of treatment with topical steroids in psoriasis? why is this?

A

do not use topical steroids for > 8 weeks

they cuse skin atrophy, striae and rebound symptoms

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63
Q

which type of psoriasis can photodynamic therapy be considered 1st line?

A

guttate psoriasis

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64
Q

how can guttate psoriasis be differentiated from pityriasis rosea?

A

presence of the herald patch indicates pityriasis rosea

herald patch is the lesion of the initial eruption

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65
Q

other then in guttate psoriasis, when else is photodynamic therapy indicated?

A

more widespread, severe disease

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66
Q

what is the mechanism of action of photodynamic therapy in psoriasis?

A

aims to damage the keratinocytes DNA to halt proliferation

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67
Q

mutations in what protein can contribute to atopic dermatitis?

A

mutations in fillagrin protein

it is responsible for maintaining the waterproof, protective nature of the keratin layer

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68
Q

how does the distribution of rashes in atopic dermatitis differ between infants and children and adults

A

infants: usually affects extensor surfaces

children and adults: usually affects flexor surfaces (wrist, cubital and popliteal fossa)

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69
Q

what is the diagnostic criteria for atopic dermatitis?

A

itch +3 of:

  1. visible flexural rash or history of one
  2. personal history of atopy
  3. dry skin in the past year
  4. onset before age 2
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70
Q

which condition presents with monomorphic punched out lesions and is considered an emergency?

what is the underlying causative of this?

A

eczema herpeticum

infection caused by herpes simplex 1

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71
Q

how is eczema herpeticum treated

A

IV aciclovir

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72
Q

in which patients is eczema herpeticum commonly seen?

A

young children with existing atopic eczema

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73
Q

when should emollients be used in atopic dermatitis?

A

always! emollients should be used even if the eczema is clear!

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74
Q

what is tacrolimus? when can it be used?

A

it is an immunosuppressant (a steroid sparing agent)

can be used in patients that require continual use of oral steroids

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75
Q

which dermatitis is caused by an overgrowth of commensal yeast on the skin?

which conditions can predispose to this?

A

seborrhoeic dermatitis

its development associated with immunosuppression due to HIV or Parkinson’s

76
Q

name 2 other conditions that are associated with seborrhoeic dermatitis?

A

blepharitis and otitis externa

77
Q

what is the proper name for cradle cap in newborns?

A

seborrhoeic dermatitis

78
Q

how is seborrhoeic dermatitis managed in infants and adults?

A

infants: emollients +/- topical steroids
adults: 1st line= emollients and topical steroids

2nd line: topical ketonazole (anti-fungal)

79
Q

which type of eczema presents with a brown/red colour in the elderly? what causes the brown/red colour?

A

venous eczema

occurs in elderly patients with venous insufficiency

brown/red colour due to hemosidrin deposition

80
Q

which type of eczema develops as a result of a chronic itch?

failure of what organ can cause this?

A

discoid eczema

renal failure (uraemia causes the itch)

the rash has disc shaped lesions

81
Q

what is the difference between irritant contact and contact allergic dermatitis?

A

irritant contact: non-immune mediated form. due to repeated exposure to substances that abrade and irritate the skin

contact allergic: T4, T cell mediated hypersensitivity reaction

82
Q

when does the rash in contact allergic dermatitis occur?

A

rash occurs 48-96 hours after exposure to the antigen

83
Q

name 4 common allergens seen in contact allergic dermatitis?

A

rubber
nickel (ie- belts, jewellery)
deodorants
hairdye

84
Q

name 3 items that can cause irritant contact dermatitis?

A

soap
detergents
urine (nappy rash is a cause of irritant contact dermatitis)

85
Q

how are both irritant contact and contact irritant dermatitis managed?

A

antigen avoidance (identified via patch testing)

regular emollients

topical steroids during flare ups

86
Q

in which type of dermatitis are patients usually builders, mechanics or hairdressers?

A

contact allergic dermatitis

87
Q

name the 4 pathological changes seen in acne vulgaris?

A
  1. duct occlusion (black and white heads)
  2. increased sebum production
  3. bacterial colonisation
  4. duct rupture
88
Q

which 2 endocrine disorders are risk factors for acne vulgaris?

A

PCOS

hyper androgenism

89
Q

what differentiates moderate acne from severe acne?

A

severe acne has cysts, nodules and significant scarring

90
Q

in acne treatment, what should benzoyl peroxide or topical retinoid always be prescribed alongside? why?

A

should always be prescribed with an oral antibiotic to reduce resistance

but… dont use topical and oral antibiotics together

91
Q

what is the 1st sign of acne rosacea? what can it be triggered by?

A

facial flushing is 1st sign

can be triggered by spicy food, alcohol, hot drinks, stress

92
Q

what is 1st line treatment for acne rosacea?

A

topical metronidazole

93
Q

what is 2nd line treatment for acne rosacea?

A

topical therapies and oral doxycycline

94
Q

in acne rosacea patients with rhinopehyma and telangiectasia, what treatment can be offered?

A

laser therapy

95
Q

what condition does lichen planus have an association with?

A

Hep C

96
Q

describe the distribution of lichen planus (flexor or extensor?)

A

affects flexor surfaces of wrist, forearm, ankles and oral mucosa

97
Q

describe the rash in lichen planus?

A

it can occur at the site of trauma

intensely itchy purple, flat topped papule or plaques

+/- lacy white mouth markings

98
Q

how is lichen planus managed?

A

potent topical steroid and anti-histamine

99
Q

what is the most common genetic skin condition?

how is it inherited?

A

tuberous sclerosis

autosomal dominant inheritance

100
Q

what are ash leaf macules? in what condition are they seen?

A

oval shaped areas of hypopigmentation

seen in tuberous sclerosis

101
Q 
which skin condition presents with: 
shagreen patches 
ash leaf macules
perigungual fibroma 
sebaceous adenoma
A

tuberous sclerosis

102
Q

how many cafe au lait macules are needed to diagnose NFB type 1?

A

> 6 macules need to be present

103
Q

the chance of developing which eye condition is very high in those with port wine stain birth marks?

A

glaucoma

104
Q

erythema multiform major is also known by what names?

A

Steven Johnstone syndrome or toxic epidermal necrolysis

105
Q

what is the most common cause of erythema multiforme?

A

herpes virus

106
Q

describe the lesion seen in erythema multiforme?

A

target lesion

ring shaped macules that are raised with a red rim and centre, with a wedge of normal skin in between

107
Q

where does erythema multiforme start and where does it spread to?

A

starts in hands, spreads to torso and upper limbs

108
Q

what is the main difference between erythema multiforme minor and major?

A

EM minor does not have mucosal involvement, EM major does

109
Q

what is erythema multiforme caused by?

A

type 4 HS reaction

cytotoxic T cells attack the basal cells in skin

110
Q

how is erythema multiforme managed?

A

supportively

treat with steroids and acyclovir if needed

111
Q

what is the differentiating factor between SJS and TEN?

A

the main differentiating factor is the extent of skin involvement:

SJS: < 10% of skin involvement

TEN: > 30% skin involvement

112
Q

in SJS/TEN, what happens if the blisters merge?

A

they undergo necrosis and large sheets of skin are lost

it can be life threatening

113
Q

what is the most common cause of SJS/ TEN?

A

most commonly caused by drug interactions

114
Q

which 3 drug classes are most likely to cause SJS/TEN?

A
  1. NSAIDs
  2. Penicillins
  3. anticonvulsants: lamotrigine, valproate
115
Q

what are seborrhoeic keratoses?

A

benign proliferations of epidermal keratinocytes

116
Q

how are seborrhoeic keratoses managed?

A

non surgical- cryotherapy, curettage

117
Q

what benign skin lesion is also known as a sun spot or liver spot?

A

actinic lentinges

118
Q

describe the pathophysiology of actininc lentinges?

A

occur due to sun exposure

due to excessive proliferation of melanocytes as a protective mechanism

119
Q

which benign lesion presents as firm, hyper pigmented papule +/- itch and pain?

it’s development is associated with trauma such as insect bite

A

dermatofibroma

120
Q

what name is given to a capillary haemangioma that develops at the site of trauma, especially on fingers?

A

pyogenic granuloma

121
Q

which is the most common skin cancer and least dangerous type of skin cancer?

A

BCC

122
Q

compare the ability to metastasise in BCC vs SCC

A

BCC: rarely metastasise but can be locally destructive

SCC: can metastasise

123
Q

compare the sun damage characteristically required in BCC vs SCC?

A

BCC: intermittent sun damage during childhood

SCC: cumulative, chronic sun damage over the years

124
Q

compare management for BCC vs SCC

A

BCC: conservative, surgical or medical (topical imiquimod)

SCC: screen for mets, surgery or topical 5-fluorouracil

125
Q

post transplant patients are at risk of which skin cancer?

A

squamous cell carcinoma

the immunosuppressants they are on are a risk factor for SCC

126
Q

describe the lesions in BCC vs SCC?

A

BCC: slow growing, pearly shine, rolled edges, central ulceration

SCC: scale, crust, bleeding, ulceration, itch and tender plaque on sun exposed area

SCC just sounds more nasty

127
Q

what makes Bowens disease different from SCC?

A

it is a full thickness dysplasia within the epidermis

unlike SCCs, it has not broken through into the dermis

128
Q

how is Bowens disease managed?

A

surgical excision/cryo/curettage

medical: photodynamic therapy, topical imiquimod

129
Q

in melanoma, what is the initial growth phase called?

A

horizontal/radial growth phase- the melanoma grows within the epidermis horizontally

there is no risk of metastasis

130
Q

which growth phase in melanomas has a risk of metastasis?

A

vertical growth phase

risk of mets once it invades the dermis

131
Q

what is the most common type of melanoma?

A

superficial spreading

has a relatively long radial (horizontal) growth phase so a low risk of metastasis

132
Q

which type of melanoma has the worst prognosis? why?

A

nodular melanoma

it goes straight into vertical growth phase so a higher risk of metastasis

133
Q

describe the differences in appearance of nodular and superficial spreading melanomas?

A

nodular: red or black lump that oozes or bleeds

superficial spreading: like a growing mole

134
Q

what type of skin cancer can result from a dysplastic naevi?

A

melanoma

135
Q

what makes up the ABCDE of clinical assessment of PIGMENTED skin lesions?

A 
A- asymmetry 
B - borders (regular or irreg) 
C- colour (uniform or variable) 
D - diameter 
E - elevation and evolution
136
Q

which type of cancer is most likely in a patient who has noticed a change in one of their moles?

A

melanoma

137
Q

which dermatological condition is associated with large joint arthritis, ulcerative colitis and sacroilitis?

A

pyoderma gangrenosum

138
Q

what is the single most important prognostic factor in melanoma?

A

the depth of the lesion

measured using breslow thickness

139
Q

what long term regime can be used to keep psoriasis under control?

A

topical calcipqotriol (vitamin D analogue)

140
Q

what values are classed as a “normal” ABPI?

what value of ABPI indicates arterial disease

A

normal: 0.9-1.2

arterial disease: <0.9

141
Q

what is a keloid scar

A

a tumour like lesion that arises from the connective tissue of a scar and extend beyond the normal dimensions of the wound

142
Q

which neurological disorder is associated with seborrhoeic dermatitis?

A

Parkinson’s disease

143
Q

which areas of the body are affected by pompholyx eczema?

A

there is an intensely itchy rash on the palms and soles

144
Q

what investigation would confirm the diagnosis of dermatitis herpetiformis?

A

diagnostic biopsy with immuniflourescence

145
Q

a description of short lived itchy lesions that are red and slightly swollen is most likely to be what condition?

A

urticaria

146
Q

what is the most appropriate treatment option for Bowen’s disease (an in-situ SSC)?

A

non surgically

topical 5 fluoro-uracil

147
Q

in what condition is a heliotrope rash seen?

A

dermatomyositis

148
Q

ash leaf macules are associated with which condition?

A

tuberous sclerosis

149
Q

which skin condition causes itchy grey irregular tracks in between the digits of both hands?

A

scabies

150
Q

how is scabies treated?

A

the patient and all close contacts treated with permethrin cream

151
Q

what are the 3 D’s seen in pellagra?

A

dementia
diarrhoea
dermatitis

152
Q

pellagra is due to what deficiency ?

A

vitamin B3 deficiency

nicotinic acid

153
Q

which condition causes a “ruddy complexion”, gout and peptic ulcer disease?

A

polycythemia

154
Q

which subtype of melanoma can extend into the nail bed and cause cause nail plate pigmentation?

A

aural lentiginous melanoma

155
Q

where in the body are BCCs usually localised to?

A

face, scalp, nose or ear

156
Q

compare the distributions of vitiligo and pityriasis versicolour?

A

vitiligo more likely to affect the trunk

pityriasis versicolour more likely to affect peripheries

157
Q

what age group does pityriasis rosea most commonly affect?

A

tends to affect young adults

158
Q

which UV band has the longest wavelength and penetrates window glass?

A

UVA

159
Q

describe the relationship between the wavelength of the UV band and the energy it carries?

A

the shorter the wavelength, the higher the energy

the more energy carried, the more it is biologically active

160
Q

describe the relationship between the wavelength of the UV band and the energy it carries?

A

the shorter the wavelength, the higher the energy

the more energy carried, the more it is biologically active

161
Q

describe the presentation of polymorphic light eruption?

A

delayed onset of vesicles and papules, non scarring

occurs in response to light

162
Q

how is polymorphic light eruption different to prickly heat?

A

both look similar

PLE occurs in response to light, prickly heat occurs in response to heat

163
Q

name the 3 drugs that are most commonly seen as the cause of drug induced photosensitivity

A

thiazides, doxycycline, naproxen

164
Q

what is the most common cause of acanthosis nigricans

A

diabetes

165
Q

both SLE and rosacea cause a rash on the face; how can they be differentiated?

A

SLE: rash spares the naso-labial folds

rosacea: rash does not spare the nano labial folds

166
Q

what must all patients >40y/o with dermatomyositis be screened for?

A

cancer

167
Q

in addition to cancer, what else are patients with dermatomyositis or polymyositis at risk of?

A

interstitial lung disease

168
Q

name 2 main dermatological manifestations of dermatomyositis?

A
  1. heliotrope rash- an erythematous rash over the upper eyelids
  2. Gottron’s papules - erythematous/violaceous papules over the extensor surface of the joints of the hand
169
Q

what electrolyte abnormality do patients with erythema nodosum commonly have?

A

hypercalcemia

170
Q

which 3 drug classes most commonly cause TEN/SJS?

A
  1. penicillins
  2. NSAIDs
  3. anti-convulsants
171
Q

which enzyme is deficient in acute intermittent porphyria?

A

porphobilinogen deaminase

172
Q

describe 3 presenting features of acute intermittent porphyria

A

usually women in their 30’s:

  • acute abdomen
  • neurological symptoms
  • mood disturbance
173
Q

what is the most common type of porphyria?

A

porphyria cutanea tarda

174
Q

which enzyme is deficient in porphyria cutanea tarda?

A

uroporphyrinogen decarboxylase

175
Q

who is most commonly affected by porphyria cutanea tarda?

A

middle aged men with liver disease

176
Q

which porphyria is classically associated with children who scream when they are placed outside in the sun and has no evident rash?

A

erythropoietic protopohphyria

177
Q

which enzyme is deficient in erythropoietic protopohphyria?

A

ferrochelatase

178
Q

what is gold standard investigation for allergy

A

skin prick testing

179
Q

in a patient with erythroderma, what clinical sign would warrant an immediate review by dermatology? why?

A

if patient develops SOB

it can be indicative of dehydration and high output heart failure

180
Q

what blood test will be significantly raised in patients with giant cell arteritis?

A

massively raised ESR

181
Q

which type of large vessel vasculitis affects branches of the aortic arch, so can cause weakened or absent pulses?

A

takaysu arteritis

182
Q

what is the most common medium vessel vasculitis that affects the coronary arteries in kids <5 y/o?

A

Kawasaki disease

183
Q

what do kids with Kawasaki disease present with?

A

fever, rash, swollen glands and red toes and eyes

184
Q

which medium vessel vasculitis is most likely to occur in a young male smoker who has previously had his fingers amputated?

A

buerger’s disease

causes clots in the vessels supplying fingers and toes

185
Q

compare how GPA and eGPA affect the nose and sinuses?

A

GPA causes sinusitis and blood mucous

eGPA does not affect the nose and sinus. there is also no granulomas present in vessel walls, unlike GPA

186
Q

how is henoch-schonlein purpura managed?

A

mostly self limiting, steroids only used if symptoms severe

AA Y4 Finals cards NE (40 decks)

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